Document Type : Original Article

Authors

1 Department of Immunology & Microbiology, School of Medicine, Arak University of Medical Sciences, Arak, Iran

2 Traditional and Complementary Medicine Research Center (TCMRC), Arak University of Medical Sciences, Arak, Iran

3 Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran

4 Infectious Diseases Research Center (IDRC), Arak University of Medical Sciences, Arak, Iran

Abstract

 
 Background: Patients with type 2 diabetes mellitus (T2DM) often have imbalance in inflammatory cells, increased inflammatory cytokines, and defects in homeostasis. The present study aimed to evaluate the percentage of Treg cells, lymphocytes, T cells, and T helper cells and the expression of the TGF-β cytokine gene in T2DM patients.
Methods : This study was conducted on 50 patients with T2DM and 50 healthy controls according to the inclusion criteria. The percentage of Treg cells, T cells, and T helper cells was determined by flow cytometry. Also, the expression of the CD4, CD25, and FOXP3 markers of Treg cells was examined. The gene expression of TGF-β cytokine was evaluated by real-time polymerase chain reaction (PCR).
Results: The percentage of Treg cells was significantly lower in patients with T2DM than in healthy controls. The number of T helper cells and lymphocytes decreased in T2DM patients as compared to the healthy controls. Based on the results, the percentage of T cells was higher in T2DM patients than in healthy controls. The expression of CD25 and FOXP3 markers in Treg cells significantly decreased in T2DM patients compared to the healthy controls; however, this decrease was not significant for the CD4 marker. Conversely, the expression of the cytokine TGF-β increased in patients with T2DM compared to the healthy controls.
Conclusion: The expression of TGF-β and the percentage of CD4 + CD25 + regulatory T cells were impaired in patients with T2DM.

Highlights

Nazanin Shahnoruzi(google scholar)(pubmed)

Mehdi SalehiNazanin Shahnoruzi(google scholar)(pubmed)

Ali Ganji(google scholar)(pubmed)

Ghasem Mosayebi(google scholar)(pubmed)

Ali Ghazavi(google scholar)(pubmed)

Keywords

Main Subjects

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